One of the academic presentations reflecting the Academic activity at Grande International Hospital, Dhapasi, Kathmandu; an initiative of our HOD of ED, Dr. Ajay Singh Thapa.

1. Respiratory Physiology
Presented by:
Dr. Pravin Prasad
Medical officer, ED
Grande International Hospital
Academic Session I
Supervisor:
Dr. Ajay Singh Thapa
Head of Department, ED
Grande International Hospital

2. Discussion Topics
• Lung Mechanics: 13 slides
• Alveolar-Blood Gas Exchange: 5 slides
• Transport of O2 and CO2: 4 slides
• Regulation of Respiration: 4 slides
• Hypoxemia and its types: 8 slides

3. Respiratory Physiology
Lung Mechanics

4. Volumes and Capacities of Lung
4 volumes:
Tidal volume
Inspiratory reserve volume
Expiratory Reserve Volume
Residual Volume
4 capacities:
Functional residual capacity
Vital capacity
Total Lung Capacity
Inspiratory
Reserve
Volume
Lung mechanic

5. Ventilation
• Total Ventilation
▫ Total volume of air moved in or out of the lungs per
minute
• Alveolar ventilation
▫ Represents room air delivered to the respiratory zone
per minute
• Why the gap??
▫ Anatomic Dead space is the space in the respiratory
system prior to the respiratory zone
*Physiological Dead Space= Anatomic dead space +
Alveolar dead space

6. Lung Mechanics
• Muscles of Respiration
▫ Inspiration: diaphragm
▫ Expiration: primarily passive process; abdominal
muscles
• Forces acting on Lung System
▫ Intra-pleural pressure, Intra-alveolar pressure
▫ Lung Recoil (tissue collagen/elastins, surface
tension: Laplace law)

7. Mechanics Under Resting Condition
During
Inspiration
Before During End Of
Intra pleural Pressure
(cm H2O)
-5 More negative
less than -5
-8
Lung Recoil Force
(cm H2O)
5 More positive
More than 5
8
Alveolar Pressure 0 slightly negative
(-1)
0
Before
Inspiration
End
Inspiration

8. Expiration??
• Passive process
• Relaxation of inspiratory muscles returns intra-
pleural pressure to -5 cm H2O
• Followed by lung deflation, driven by lung recoil
till it becomes equal to intra-pleural pressure
• Smaller alveoli containing larger amount of
gases: intra-alveolar pressure increases
• Air flows outside and the intra-alveolar pressure
becomes zero.

9. Intra-pleural and Intra-alveolar
pressures during respiration

10. Intra-pleural and Intra-alveolar
pressures: Applied Part
• Pneumo-thorax
• Positive Pressure Ventilation
▫ Assisted Control Mode Ventilation
▫ Positive End Expiration Pressure

11. Lung Recoil
• Tissue Elastins/ Collagens
• Surface Tension: Laplace Law
• Role of Surfactant??
▫ Decrease surface tension
▫ Bias the surface tension
▫ Reduce the chance of pulmonary edema

12. Surfactant: Applied Aspects
• Respiratory Distress Syndrome
• Atelectasis
• Pulmonary Edema

13. Lung Compliance
• Is the unit change in lung volume for unit change in
pressure.
• Has 2 components:
▫ steeper part (higher compliance)
▫ flatter part (lower compliance)

14. Forced Vital Capacity, Forced
Expiratory Volume in 1st second, and
their applied aspects

15. Pulmonary Function Tests: Comparison
Obstructive
pattern
Restrictive
Pattern
Total Lung Capacity  
Forced Expiratory
Volume in 1st second
(FEV1)
 
Forced Vital Capacity
(FVC)
 
FEV1/FVC   Or Normal
Peak Flow 
Functional Residual
Capacity (FRC)
 
Residual Volume  

16. Respiratory Physiology
Alveolar-Blood Gas Exchange

17. Alveolar Blood Gas Exchange
• Partial Pressure of a gas in ambient air:
▫ Pgas= Fgas x Patm
• Partial Pressure of a gas in inspired air:
▫ PIgas = Fgas (Patm-PH2O)
• Partial Pressure of a gas in alveoli:
▫ PAgas = Fgas(Patm – PH2O)-PAother gases

18. Alveolar Blood Gas Exchange

19. Factors Affecting Alveolar CO2
Concentration
• CO2
▫ PACO2 
▫ Increases with increasing CO2 production
(increased metabolism)
▫ Inverse relation with alveolar ventilation
 Hyperventilation: doubled ventilation, PACO2
decreases by half
 Hypoventilation: halved ventilation, PACO2
doubled
metabolic CO2 production
alveolar ventilation

20. Factors Affecting Alveolar O2
Concentration
• PAO2 = FO2
(Patm –PH2O)-(PACO2/RR)
▫ RR: respiratory ratio =CO2 produced ml/min
O2 consumed ml/min

21. ALVEOLAR-BLOOD GAS TRANSFER:
FICK LAW OF DIFFUSION
• Vgas = A/T x D x (P1-P2)
• Factors affecting rate of diffusion:
▫ Structural factors:
a. Surface area for exchange:  in emphysema,  in
exercise
b. Thickness of membranes between alveolar gas
and capillary blood.
▫ Factors specific to each gas present:
a. Diffusion constant: solubility clinically significant
b. Gradient across the membrane

22. Respiratory Physiology
Transport of O2 and CO2

23. Transport of Gases:
Introduction
• Down hill flow
▫ O2: From the alveoli to the tissues,
▫ CO2: From the tissues to the alveoli
• Transportation made feasible by:
▫ Combined with the gas- carrying protein: O2 with
hemoglobin (Hb)(99%), increase transportation by 70
fold
▫ Series of reversible chemical reactions that convert
gases into other compounds: CO2, increase
transportation by 17 fold

24. TRANSPORT OF OXYGEN
• Transported as:
▫ Dissolved form
▫ Combined with Hb

• 1 gm Hb combines with
1.34 mL of O2
• Normal Hb
concentration: 15 mg
/dL
• Total O2 carried with
Hb: 1.34 x 15=20 mL
O2/100 mL of blood

25. Shifts of Oxygen-Dissociation Curve
• Bohr Effect:
• Decreased affinity of Hb
for O2 with acidic pH

26. Transport of Carbon Dioxide
Plasma RBC
In Dissolved form
(0.3mL%)
•As dissolved solution
(0.1mL%)
•As carbonic acid
((0.2mL%)
•As Carbonic Acid
(0.1mL%)
As carbamino
compounds
(0.7mL%)
•As carbamino-proteins
(0.1mL%)
•As carbamino-
haemoglobin (0.6mL%)
As bicarbonates
(3mL%)
•As NaHCO3 (2.1mL%)
•By phosphate buffer
•By protein reduction
•As KHCO3 (0.9mL%)

27. Transport of Carbon dioxide
• Haldane Effect:
▫ Increased capacity of deoxygenated Hb to bind
and carry CO2 resulting in facilitated CO2
 binding at tissue level
 transport in venous blood
 release in alveoli
• Chloride Shift

28. Respiratory Acidosis and Alkalosis
• Respiratory acidosis:
▫ pH decreases
▫ Increased arterial PCO2
▫ Compensation: excretion of H+ ion and retention
of HCO3
- ions by kidneys
• Respiratory alkalosis:
▫ pH increases
▫ Decreased arterial PCO2
▫ Compensation: retention of H+ ion and excretion
of HCO3
- ions by kidneys

29. Metabolic Acidosis and Alkalosis
• Metabolic Acidosis:
▫ Decrease in pH
▫ Strong acids added to blood, H+ ions fixed by
generation of H2CO3, dissociates in to H2O and
CO2, CO2 removed by lungs: rapid process
▫ No change in PCO2
▫ Compensation: increased ventilation to remove
PCO2, returning pH to normal
• Metabolic Alkalosis: ??

30. Respiratory Physiology
Regulation of Respiration

31. Control Systems
• Neural Control:
▫ Medullary Control:
 Pre-Botzinger complex (pre-BOTC)
 Rhythmic discharges passed through phrenic nerves
 NK1 receptors and μ-opioid receptors on these neurons:
substance P stimulates and opioids inhibit respiration
 Dorsal and Ventral groups of respiratory neurons
 Efferents to pre-BOTC
▫ Pontine Control:
 Puenmotaxic center (Nucleus parabrachialis, NPBL)
 Inspiratory areas and Expiratory areas
 Afferents from lungs and airways: via vagus nerve.
 Efferents: Medulla

32. Neural Centers for Respiratory control

33. Receptors
• Central Chemo-receptors
▫ Stimulated by CSF [H+] and CO2
▫ Adaptation occurs
▫ Insensitive to PO2 and arterial H+
• Peripheral Chemo-receptors
▫ Carotid bodies:
 near carotid sinus, afferents to CN IX
▫ Aortic bodies:
 Aortic arch, afferents to CN X
▫ Contains:
 H+/CO2 receptors: less sensitive, but maintains the normal
drive.
 Po2 receptors: responds to PO2 (dissolved O2) and not to total
oxygen content(bound to Hb).
 Do not contribute to normal drive.
 Activated if PaO2 <50-60 mmHg
▫ Do not adapt.

34. Peripheral Chemoreceptors

35. Respiratory Physiology
Hypoxemia

36. Hypoxia
• Hypoxic Hypoxia (Hypoxemia): reduced arterial
PO2
• Anaemic Hypoxia: normal arterial PO2,
decreased carriers (Hb)
• Ischaemic/stagnant Hypoxia: normal arterial
Po2 and Hb, decreased blood flow to tissues
• Histotoxic Hypoxia: normal arterial Po2 and Hb,
normal flow to the tissues, tissues can’t utilize
the delivered O2

37. Hypoxemia: Four Prime Causes
• Ventilation-Perfusion (VA/Q) mismatch
• Hypoventilation
• Diffusion impairment
• Pulmonary shunt

38. Ventilation-Perfusion Mismatch
• Regional Differences in Ventilation
▫ Due to effects of gravity over intra-plueral fluid
column.
• Regional differences in Perfusion
▫ Gravity
▫ Pulmonary artery diameter

39. Regional Differences in Ventilation
A t the Apex At the Base
At rest Lower Pressure (More negative)
Alveoli relatively distended
Higher Pressure (Less negative)
Alveoli relatively small
During
Inspiration
Alveoli receives less air (poor
ventilation)
Alveoli receives more air (better
ventilation)

40. Regional Differences in Perfusion
At Apex At Base
Pulmonary arterial
pressure (mainly due to
gravity)
Decreases Increases
Vessels diameter (relative
hypoxia) And
Resistance
Relatively constricted
High resistance
Relatively dilated
Low resistance
Blood Flow Low High

41. Ventilation-Perfusion Relationships
At Apex At Base
Ventilation Low High
Perfusion Low High
Relatively VA/Q ratio Over ventilated Under ventilated

42. Hypoventilation
In normal condition:
• Alveolar PCO2(PACO2): 40 mmHg and
Alveolar PO2 (PAO2): 100 mmHg
• Equilibrium between alveolar and
pulmonary capillary partial pressures
• Due to VA/Q mismatch, systemic PO2
(PaO2): 95mmHg
• A-a gradient: 5-10 mmHg
During Hypoventilation(for example):
• Alveolar PCO2(PACO2): 80 mmHg and
Alveolar PO2 (PAO2): 60 mmHg
• Equilibrium between alveolar and
pulmonary capillary partial pressures
• Due to VA/Q mismatch, systemic PO2
(PaO2): 55mmHg
• A-a gradient: 5-10 mmHg (i.e.
NORMAL)

43. Diffusion Impairment
• Structural Problem in the lungs
− Decreased surface area (A)
− Increased thickness of lung membrane (T)
For Diffusion Impairment:
• Alveolar PO2 (PAO2): 100 mmHg
• Mismatch between alveolar and
pulmonary capillary partial pressures
i.e. PO2 < PAO2
• Due to VA/Q and alveolar-capillary
mismatch, systemic PO2 (PaO2):
95mmHg
• A-a gradient: increases
• Solution: Increase gradient to facilitate
diffusion.

44. Pulmonary shunt

45. Respiratory Physiology
Recommendations

46. Respiratory Physiology
Thank you!!